Phospholipid metabolism will be studied in lung from late fetal and early neonatal offspring of streptozotocin diabetic rats and offspring of normal animals. Amounts and fatty acid composition of phospholipids and amounts and nature of phospholipid remodeling/precursor fragments will be measured using HPLC of acid soluble phosphates and of lipid soluble phospholipids, and a unique automated phosphate analyzing machine developed in these laboratories. HPLC will be combined with GLC for fatty acyl identification. Incorporation of 33 Pi into the phosphates will be measured simultaneously with estimation of the amounts of phosphates. Incorporatin of 3H- and of 14C substrates (e.g., choline, ethanolamine, fatty acids, glucose, etc.) into phosphates will also be measured. The influence of insulin and of glucocorticoid administration to the mothers upon fetal and neonatal lung phosphate metabolism will be investigated. We hope to identify whether deranged phospholipid metabolism, especially at the level of remodeling is a sequela of maternal diabetes. Information is particularly sought with regard to the minor phospholipids. Since glucose is a prime substrate for pulmonary phospholipid synthesis we hypothesize that normal channelling of glucose into glycogen synthesis, glycogenolysis, glycolysis and through the hexose monophosphate shunt, might be misdirected in the developing lung of infants of diabetic mothers. Data we will obtain on phospholipids per se, on phospholipid remodelling fragments and on the phosphorylated esters of glycolysis, the nucleotides and creatine phosphate will help clarify this area.